This proposal intends to examine the cellular basis of defective immunoregulation in patients with acute and chronic active hepatitus (CAH). Our studies are design to determine if there exists aberrancies in regulatory cell populations or altered intrinsic effector cells resistance to normal homeostatic control populations. If aberrant regulatory cell populations are delineated in CAH with persistent hypergammaglobulinemia, the nature and role of soluble mediators from isolated subpopulations will be examined. The overall aim of this study is to characterized the cellular basis of abnormal B cell function in human hepatitis. The specific aims include. 1) To detemine if the B cell hyperactivity represents defects of intrinsic effector cells or alterations in extrinsic regulatory cell subpopulations. 2). To characterize the aberrant subpopulation(s) by cell surface markers. 3) Attempt to define the role of soluble mediators from highly purified aberrant subpopulations.